Bottom Line:
Currently there has been no effective treatment of diabetic encephalopathy.The results showed that 8 weeks of Radix Polygoni Multiflori treatment could improve the cognitive dysfunction of diabetic rats (P < 0.01), recover the ultrastructure of hippocampal neurons, and increase the number of synapses in a dose-dependent manner.Further experiment also suggested that the neuroprotective effect of Radix Polygoni Multiflori was partly achieved by downregulating MLCK expression in hippocampus via ERK signaling.

ABSTRACTCurrently there has been no effective treatment of diabetic encephalopathy. Radix Polygoni Multiflori, a famous traditional Chinese medicine, is widely used in antiaging treatment, especially in prevention and treatment of Alzheimer's diseases. In this study we tried to explore the effect of Radix Polygoni Multiflori on cognitive function among diabetic rats with demonstrated cognitive impairment. SD rats were divided into group A (control group), group B (diabetes), group C (treated with Radix Polygoni Multiflori at the dose of 2 g/kg/d), and group D (treated with same drug at the dose of 1 g/kg/d). The results showed that 8 weeks of Radix Polygoni Multiflori treatment could improve the cognitive dysfunction of diabetic rats (P < 0.01), recover the ultrastructure of hippocampal neurons, and increase the number of synapses in a dose-dependent manner. Further experiment also suggested that the neuroprotective effect of Radix Polygoni Multiflori was partly achieved by downregulating MLCK expression in hippocampus via ERK signaling.

fig2: The representative photos of MLCK (red light) and NMDAR2B (green light) expressions in hippocampal tissue in rats by immunofluorescence staining. The coexpression of MLCK and NMDAR2B was shown as yellow light. (A1)–(A3), control rats; (B1)–(B3), diabetic rats. Immunofluorescence staining showed that the expression of MLCK and the NMDA receptor and their coexpression in the rats hippocampus in diabetic rats (group B) were significantly higher than rats in control rats (group A) (P < 0.05) (Figure 2, Supplementary Table 1). According to the Person correlation analysis, the expression of MLCK and NMDAR2B showed a positive correlation (r = 0.958, P < 0.01) (Supplementary Figure 1).

Mentions:
Immunofluorescence staining showed that the expression of MLCK and the NMDA receptor in the rats hippocampus in group B was significantly higher than rats in group A. Coexpression of MLCK and NMDA receptor was also significantly higher than that in group A, which showed a statistically significant difference (P < 0.05) (Figure 2, Supplementary Table 1 in Supplementary Material available online at http://dx.doi.org/10.1155/2015/484721, the expression of MLCK showed in red fluorescence, the expression of NMDAR2B in green fluorescence, and the coexpression in yellow fluorescence.). According to the Pearson correlation analysis, the expression of MLCK and NMDAR2B showed a positive correlation (r = 0.958, P < 0.01) (Supplementary Figure 1).

fig2: The representative photos of MLCK (red light) and NMDAR2B (green light) expressions in hippocampal tissue in rats by immunofluorescence staining. The coexpression of MLCK and NMDAR2B was shown as yellow light. (A1)–(A3), control rats; (B1)–(B3), diabetic rats. Immunofluorescence staining showed that the expression of MLCK and the NMDA receptor and their coexpression in the rats hippocampus in diabetic rats (group B) were significantly higher than rats in control rats (group A) (P < 0.05) (Figure 2, Supplementary Table 1). According to the Person correlation analysis, the expression of MLCK and NMDAR2B showed a positive correlation (r = 0.958, P < 0.01) (Supplementary Figure 1).

Mentions:
Immunofluorescence staining showed that the expression of MLCK and the NMDA receptor in the rats hippocampus in group B was significantly higher than rats in group A. Coexpression of MLCK and NMDA receptor was also significantly higher than that in group A, which showed a statistically significant difference (P < 0.05) (Figure 2, Supplementary Table 1 in Supplementary Material available online at http://dx.doi.org/10.1155/2015/484721, the expression of MLCK showed in red fluorescence, the expression of NMDAR2B in green fluorescence, and the coexpression in yellow fluorescence.). According to the Pearson correlation analysis, the expression of MLCK and NMDAR2B showed a positive correlation (r = 0.958, P < 0.01) (Supplementary Figure 1).

Bottom Line:
Currently there has been no effective treatment of diabetic encephalopathy.The results showed that 8 weeks of Radix Polygoni Multiflori treatment could improve the cognitive dysfunction of diabetic rats (P < 0.01), recover the ultrastructure of hippocampal neurons, and increase the number of synapses in a dose-dependent manner.Further experiment also suggested that the neuroprotective effect of Radix Polygoni Multiflori was partly achieved by downregulating MLCK expression in hippocampus via ERK signaling.

ABSTRACTCurrently there has been no effective treatment of diabetic encephalopathy. Radix Polygoni Multiflori, a famous traditional Chinese medicine, is widely used in antiaging treatment, especially in prevention and treatment of Alzheimer's diseases. In this study we tried to explore the effect of Radix Polygoni Multiflori on cognitive function among diabetic rats with demonstrated cognitive impairment. SD rats were divided into group A (control group), group B (diabetes), group C (treated with Radix Polygoni Multiflori at the dose of 2 g/kg/d), and group D (treated with same drug at the dose of 1 g/kg/d). The results showed that 8 weeks of Radix Polygoni Multiflori treatment could improve the cognitive dysfunction of diabetic rats (P < 0.01), recover the ultrastructure of hippocampal neurons, and increase the number of synapses in a dose-dependent manner. Further experiment also suggested that the neuroprotective effect of Radix Polygoni Multiflori was partly achieved by downregulating MLCK expression in hippocampus via ERK signaling.